Literatura científica selecionada sobre o tema "Protection Cardiaque"
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Artigos de revistas sobre o assunto "Protection Cardiaque"
Lanclas, H., S. Ricômes, J. Fichet e A. Cariou. "L’arrêt cardiaque — Protection cérébrale post-arrêt cardiaque". Réanimation 20, S2 (28 de dezembro de 2010): 621–29. http://dx.doi.org/10.1007/s13546-010-0038-9.
Texto completo da fonteBaumgartner e Georgiadis. "Sekundärprävention nach ischämischem Schlaganfall". Praxis 92, n.º 5 (1 de janeiro de 2003): 168–78. http://dx.doi.org/10.1024/0369-8394.92.5.168.
Texto completo da fonteMartin, S., e R. Andriantsitohaina. "Mécanismes de la protection cardiaque et vasculaire des polyphénols au niveau de l’endothélium". Annales de Cardiologie et d'Angéiologie 51, n.º 6 (dezembro de 2002): 304–15. http://dx.doi.org/10.1016/s0003-3928(02)00138-5.
Texto completo da fonteMassy, Ziad A. "Étude SHARP Étude de protection cardiaque et rénale chez des patients insuffisants rénaux chroniques". Néphrologie & Thérapeutique 1, n.º 3 (julho de 2005): 204–5. http://dx.doi.org/10.1016/j.nephro.2005.05.007.
Texto completo da fonteCaillard, S. "Bénéfices des inhibiteurs du signal de prolifération au-delà de l’immunosuppression. Protection vasculaire et expérience en transplantation cardiaque". Néphrologie & Thérapeutique 5 (dezembro de 2009): S379—S384. http://dx.doi.org/10.1016/s1769-7255(09)73429-7.
Texto completo da fonteGeoffroy, P. A. "Les objets connectés sont-ils le futur de la sémiologie psychiatrique ?" European Psychiatry 30, S2 (novembro de 2015): S78. http://dx.doi.org/10.1016/j.eurpsy.2015.09.353.
Texto completo da fonteAmraoui, Jibba, Lauriane Bordenave, Gilles Leclerc, Geneviève Salvignol, Marta Jarlier, Catherine Fiess, Laurent Philibert, Régis Fuzier e Célia Touraine. "Benefits of cardiac coherence combined with medical hypnosis on preoperative anxiety before cancer surgery: the COHEC II study trial protocol". BMJ Open 13, n.º 12 (dezembro de 2023): e072215. http://dx.doi.org/10.1136/bmjopen-2023-072215.
Texto completo da fonteQuidelleur, E., B. Loddé, C. L. Igoho-Zephir, M. B. Eniafe-Eveillard, P. Choucroun, J. D. Dewitte e A. Baert. "Évaluation des contraintes physiques, environnementales et de l’astreinte cardiaque de 43 opérateurs (en tenue de protection) de la dépollution de produits pétroliers lourds". Archives des Maladies Professionnelles et de l'Environnement 70, n.º 3 (junho de 2009): 306–14. http://dx.doi.org/10.1016/j.admp.2008.12.011.
Texto completo da fonteReungoat, P., V. Lelaurain, O. Méchineau, I. Rouilleaux, C. Gonzalez, C. Lembeye e P. Brochard. "Évaluation de la contrainte cardiaque engendrée par le port d’un Appareil de protection Respiratoire de type Isolant à Circuit Ouvert (ARICO) chez 104 sapeurs-pompiers". Archives des Maladies Professionnelles et de l'Environnement 65, n.º 2-3 (maio de 2004): 245. http://dx.doi.org/10.1016/s1775-8785(04)93345-0.
Texto completo da fonteRigal, Jean-Christophe, Elodie Boissier, Karim Lakhal, Valéry-Pierre Riche, Isabelle Durand-Zaleski e Bertrand Rozec. "Cost-effectiveness of point-of-care viscoelastic haemostatic assays in the management of bleeding during cardiac surgery: protocol for a prospective multicentre pragmatic study with stepped-wedge cluster randomised controlled design and 1-year follow-up (the IMOTEC study)". BMJ Open 9, n.º 11 (novembro de 2019): e029751. http://dx.doi.org/10.1136/bmjopen-2019-029751.
Texto completo da fonteTeses / dissertações sobre o assunto "Protection Cardiaque"
Incagnoli, Pascal. "Protection tissulaire dans l'arrêt circulatoire : du massage cardiaque à la protection pharmacologique. Approche clinique et expérimentale". Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00602422.
Texto completo da fonteMichel, Pierre. "Protection du greffon cardiaque durant l'ischémie froide de la reperfusion". Lyon 1, 2002. http://www.theses.fr/2002LYO1T260.
Texto completo da fonteJegou, Bruno. "Protection myocardique en chirurgie cardiaque d'apres une revue de la litterature". Nantes, 1993. http://www.theses.fr/1993NANT253M.
Texto completo da fonteObadia, Jean-François. "La protection myocardique : de l'approche expérimentale aux applications cliniques en chirurgie cardiaque". Dijon, 1996. http://www.theses.fr/1996DIJOMU02.
Texto completo da fontePANGRANI, MARC. "L'oreillette droite : cavite cardiaque emergee et pourtant negligee dans la protection myocardique". Nice, 1992. http://www.theses.fr/1992NICE6507.
Texto completo da fonteGoldstein, JacquesPierre. "Evaluation expérimentale d'une méthode de protection myocardique au cours de l'ischémie cardiaque peropératoire". Doctoral thesis, Universite Libre de Bruxelles, 1988. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213395.
Texto completo da fonteAbadie, Claire. "La séquence ischémie-reperfusion cardiaque : incidences fonctionnelles et approches pharmacologiques de la protection myocardique". Dijon, 1994. http://www.theses.fr/1994DIJOMU01.
Texto completo da fonteMaupoint, Julie. "Mise en évidence du rôle direct de la protection endothéliale dans la modulation de l'insuffisance cardiaque". Rouen, 2017. http://www.theses.fr/2016ROUENR12.
Texto completo da fonteEndothelial dysfunction, mainly characterized by a decrease in nitric oxide production (NO), is associated with many cardiovascular diseases especially heart failure (HF), insulin resistance (IR) and type 2 diabetes. Among the mechanisms which could explain this decrease in NO production, an alteration of signaling pathways leading to activation of PI3K/Akt/eNOS (endothelial NO synthase) is likely to play a role. Indeed, this pathway is dependent on many post-translational regulations, especially phosphorylation. Upstream of this pathway, phosphorylation on tyrosine residue leads to its activation, whereas dephosphorylation by the action of protein phosphatases in particular protein tyrosine phosphatase 1B (PTP1B) decreases NO production in response to insulin and shear stress. The concept developed in our laboratory is that PTP1B inhibition could be a potential therapeutic target of HF and IR by improving both NO production and insulin sensitivity. The aggravating role of endothelial dysfunction in these contexts has been largely suggested but has never been demonstrated directly. The objective of our work is thus to demonstrate this direct link. In different models of cardiac dysfunction (post-infarction HF, aging, type 2 diabetes), we showed an improvement of endothelial function in animals that did not express endothelial PTP1B. Furthermore, in the post-infarction HF model, this selective endothelial protection resulted in a prevention of the alterations of cardiac function, remodeling and hemodynamics and resulted in an improvement of survival. Regarding the model of type 2 diabetes, we showed an endothelial protection via endothelial PTP1B inhibition, triggered an improvement of both sensibility to insulin and cardiac function / hemodynamics. This work thus allowed to demonstrate the direct role of endothelial protection on cardiac dysfunction in a model of post-infarction HF and in type 2 diabetes. They further reinforce the concept that PTP1B inhibition is a promising treatment of cardiovascular diseases
Mammadova, Aynura. "The role of MEIS inhibitors in cardiac regeneration and protection". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ006.
Texto completo da fonteThe TALE-type homeobox gene MEIS1 has been identified as a critical factor in controlling the cell cycle arrest of cardiomyocytes, presenting itself as an attractive target for therapy. Our latest investigations have revealed the potential of MEIS1 suppression to promote the regeneration of cardiomyocytes. Further experiments with neonatal cardiomyocytes showed that two innovative small molecules, MEISi-1 and MEISi-2, enhanced the proliferation (Ph3+TnnT cells) and cytokinesis (AuroraB+TnnT cells) of these cells. Suppressing MEIS1 activity resulted in the diminished expression of its target genes and the inhibitors of cyclin-dependent kinases. Additionally, this research extended to cultivating human induced pluripotent stem cells (hiPSCs) into cardiomyocytes to examine the impact of MEIS1 suppression, which notably did not compromise their viability. Intriguingly, short-term and long-term treatment with MEISi in hiPSCs led to significant elevation in essential cardiac-specific gene expression, notably influencing cardiac mesoderm and progenitor cells, and positioning MEIS1 inhibitors as crucial modulators of cardiac gene expression. Our findings indicate that MEIS inhibitors can provide protection against the acute cardiotoxic effects of doxorubicin (DOX) in Wistar rats, as evidenced by the maintained structure of cardiac tissue and unchanged levels of fibrosis or collagen. qPCR analyses further confirmed the upregulation of cardiac progenitor genes and a balance in anti-apoptotic and ROS-related gene expression, hinting at the protective role of MEIS inhibitors against DOX-induced damage without influencing fibrosis. These results highlight the therapeutic potential of MEIS inhibitors in regenerative cardiology, suggesting their utility in enhancing cardiomyocyte renewal and offering protection against cardiotoxicity
Koning, Nick Julius. "Protection of the microcirculation during cardiac surgery with cardiopulmonary bypass". Thesis, Angers, 2017. http://www.theses.fr/2017ANGE0073/document.
Texto completo da fonteCardiac surgery with cardiopulmonary bypass leads to impaired perfusion of the microcirculation, which may be an important contributor to postoperative organ dysfunction. This thesis combines clinical and animal studies that aimed to investigate the mechanisms underlying microcirculatory dysfunction in cardiac surgery with cardiopulmonary bypass. Moreover, we aimed to evaluate two treatments strategies for preservation of microcirculatory perfusion during cardiopulmonary bypass : the use of pulsatile flow as compared to the conventional non pulsatile flow during cardiopulmonary bypass and treatment with imatinib in order to reduce vascular leakage by inhibiting endothelial barrier dysfunction.The current thesis has demonstrated that microcirculatory perfusion is impaired during and after cardiac surgery, and this can be attributed mainly to inflammatory endothelial barrier dysfunction and consequent vascular leakage. Concomitant hemodilution may additionally contribute to reduced microvascular perfusion and oxygenation in on-pumpcardiac surgery. We showed that the use of pulsatile flow during cardiopulmonary bypass improves postoperative microvascular perfusion as compared to non pulsatile flow. Imatinib treatment reduced endothelial barrier dysfunction and vascular leakage in our rat model for cardiopulmonary bypass and resulted in preservation of microcirculatory perfusion andoxygenation during and after extracorporeal circulation.Moreover, imatinib treatment resulted in reduced markers ofrenal, pulmonary and intestinal injury after cardiopulmonary bypass. Based on our findings, reduction of vascular leakage and use of pulsatile flow during cardiopulmonary bypass are promising interventions for the prevention of postoperative complications in patients at risk for organ failure following cardiac surgery with cardiopulmonary bypass